Evidence map›Paper›PMID 28579323›Full record

ReviewTrends in immunology2017

Type I Interferon in Chronic Virus Infection and Cancer.

Laura M Snell, Tracy L McGaha, David G Brooks

Open access · greenAbstract readReview
In one paragraph

Review in Trends in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 316 papers.

0numbers the graph read from it
0cells of the map it votes in
316citing papers in PubMed
16.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

316 citing papers in PubMed, 502 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Formic acid released by intratumoralActa pharmaceutica Sinica. B · 2026
    Article
  6. Article
  7. Evolution ofInternational journal of molecular sciences · 2026
    Review
  8. Review
  9. Review
  10. Extracellular cGAMP in health and disease.Molecular biomedicine · 2026
    Review
  11. Mitochondrial double-stranded RNA fuels pancreatic cancer growth via RIG-I/TLR3 inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Review
  13. Irgm1 Restrains CD8European journal of immunology · 2026
    Article
  14. tRNA mCellular & molecular immunology · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

256 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Laura M SnellPrincess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada.
Tracy L McGahaPrincess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada; Department of Immunology, University of Toronto, Toronto, ONT, M5S 1A8, Canada. Electronic address: tmcgaha@uhnresearch.ca.
David G BrooksPrincess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada; Department of Immunology, University of Toronto, Toronto, ONT, M5S 1A8, Canada. Electronic address: dbrooks@uhnresearch.ca.
University of Toronto · CAPrincess Margaret Cancer Centre · CA

Funding

Mechanisms of Viral PersistenceR01AI085043 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2010 to 2023
$4.5M
The role of marginal zone macrophages and immuno-metabolism in tumor-driven MDSC developmentR01CA190449 · NCI · UNIVERSITY HEALTH NETWORK · PI MCGAHA, TRACY L · 2015 to 2020
$1.3M
Mechanistic relationships between IDO, GCN2, and mTOR signals in immunity to apoptotic cellsR01AR067763 · NIAMS · UNIVERSITY HEALTH NETWORK · PI MCGAHA, TRACY L · 2015 to 2019
$1.2M
The role of GCN2-kinase in antigen presenting cell function and tolerance to selfR21AI105500 · NIAID · AUGUSTA UNIVERSITY · PI MCGAHA, TRACY L · 2013 to 2014
$399k
CIHR FDN148386NCI NIH HHS R01 CA190449NIAID NIH HHS R01 AI085043NIAID NIH HHS R21 AI105500NIAMS NIH HHS R01 AR067763
6 · The paper itself

Abstract

Type I interferons (IFN-Is) are emerging as key drivers of inflammation and immunosuppression in chronic infection. Control of these infections requires IFN-I signaling; however, prolonged IFN-I signaling can lead to immune dysfunction. IFN-Is are also emerging as double-edged swords in cancer, providing necessary inflammatory signals, while initiating feedback suppression in both immune and cancer cells. Here, we review the proinflammatory and suppressive mechanisms potentiated by IFN-Is during chronic virus infections and discuss the similar, newly emerging dichotomy in cancer. We then discuss how this understanding is leading to new therapeutic concepts and immunotherapy combinations. We propose that, by modulating the immune response at its foundation, it may be possible to widely reshape immunity to control these chronic diseases.

Indexed as

AnimalsAntineoplastic AgentsAntiviral AgentsChronic DiseaseHumansImmune ToleranceInflammationInterferon Type INeoplasmsSignal TransductionVirus DiseasesAntineoplastic AgentsAntiviral AgentsInterferon Type IcancerCD4 T cellCD8 T cellchronic virusdendritic cellHCVHIVimmune activationimmunotherapyinnate immunityinterferon alphainterferon betaLCMVmacrophagepersistent virusT cell exhaustiontumortype I interferon

Identifiers

PMID28579323
PMCPMC8059441
OpenAlexW2621003511

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.